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류마티스관절염 활막세포에서 NF-${kappa}B$ 신호전달을 통한 MIF의 SDF-1 생성 유도
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  • 류마티스관절염 활막세포에서 NF-${kappa}B$ 신호전달을 통한 MIF의 SDF-1 생성 유도
저자명
조미라,박미경,김경운,오혜좌,이선영,박진실,허유정,주지현,민준기,이상헌,박성환,김호연,Cho. Mi-La,Park. Mi-Kyung,Kim. Kyoung-Woon,Oh. Hye-Jwa,Lee. Seon-Yeong,Park. Jin
간행물명
Immune network : official journal of the Korean association of immunobiologists
권/호정보
2007년|7권 1호|pp.39-47 (9 pages)
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Background: Stromal cell-derived factor (SDF)-1 is a potent chemoattractant for activated T cells into the inflamed Rheumatoid arthritis (RA) synovium. To determine the effect of macrophage migration inhibitory factor (MIF) on the production of SDF-1 in the inflamed RA synovium. Methods: The expression of SDF-1 and MIF in RA and Osteoarthritis (OA) synovium was examined by immunohistochemical staining. The SDF-1 was quantified by RT-PCR and ELISA after RA fibroblast like synoviocyte (FLS) were treated with MIF in the presence and absence of inhibitors of intracellular signal molecules. The synovial fluid (SF) and serum levels of MIF and SDF-1 in RA, OA and healthy control were measured by ELISA. Results: Expression of SDF-1 and MIF in synovium was higher in RA patients than in OA patients. The production of SDF-1 was enhanced in RA FLS by MIF stimulation. Such effect of MIF was blocked by the inhibitors of NF-${kappa}B$. Concentrations of SDF-1 in the serum and SF were higher in RA patients than in OA patients and healthy control. SDF-1 and MIF was overexpressed in RA FLS, and MIF could up-regulate the production of SDF-1 in RA FLS via NF-${kappa}B$-mediated pathways. Conclusion: These results suggest that an inhibition of interaction between MIF from T cells and SDF-1 of FLS may provide a new therapeutic approach in the treatment of RA.